Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MOD II > TBL 3 - Pain Management and Analgesics > Flashcards

TBL 3 - Pain Management and Analgesics Flashcards

1
Q

What drugs are considered counterirritants?

A

Capsaicin, Menthol, Methyl Salicylate, and Camphor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the mechanism of counterirritants?

A

Desensitize thermal receptors (transient receptor potential vanilloid (TRPV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What drugs are considered prostanoids?

A

Thromboxane, Prostaglandins, and Prostacyclin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What drugs use the COX-1 pathway?

A

Thromboxane and Prostaglandins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What drug uses the COX-2 pathway?

A

Prostacyclin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What drugs are considered corticosteroids?

A

Hydrocortisone, Prednisone, and Dexamethasone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the MOA of corticosteroids?

A

Inhibit phospholipase 2.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the MOA of acetaminophen (Tylenol)?

A

Unknown

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the properties of acetaminophen (Tylenol)?

A

Analgesic
Antipyretic
Lacks anti-inflammatory properties

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the role in therapy for acetaminophen (Tylenol)?

A

Opioid sparing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the adverse effect of acetaminophen (Tylenol)?

A

Hepatoxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the treatment for APAP/acetaminophen toxicity?

A

N-acetylcysteine (NAC)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the MOA of N-acetylcysteine?

A

Restores glutathione

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the MOA of NSAIDs?

A

COX inhibitors
Inhibit prostanoid synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are some adverse effects of NSAIDs?

A

GL ulcers and bleeds
CV disease
Nephrotoxicity
Bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Are NSAIDs anti-inflammatory?

A

Yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is an example of a COX-2 selective NSAID?

A

Celecoxib

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are some examples of Non-Selective NSAIDs?

A

Aspirin, Indomethacin, Meloxicam, Ibuprofen, Naproxen, Ketorolac, and Diclofenac

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the three drugs that induce the “Triple Whammy?”

A

NSAIDs + Diuretics + ACE-is

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Does aspirin reversibly or irreversibly bind COX enzymes?

A

Irreversibly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are some toxic effects of aspirin?

A

Uncouples oxidative phosphorylation leading to metabolic acidosis.

Respiratory alkalosis -> respriratory acidosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are some effects of aspirin toxicity?

A

Acidosis, tinnitus, bleeding, and altered mental status.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the treatment for aspirin toxicity?

A

Sodium bicarbonate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are some examples of Alpha-2 Agonists?

A

Clonidine, Tizanidine, and Dexmedetomidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the MOA of Alpha-2 Agonists?

A

Decreases presynaptic Ca2+ influx.
Increases postsynaptic K+ efflux.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the role in therapy for Alpha-2 Agonists?

A

Spasticity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are some adverse effects of Alpha-2 Agonists?

A

Hypotension
Bradycardia
Sedation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What does Alpha-1 Agonism cause?

A

Constriction of vascular smooth muscle, leading to increased BP.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What does Alpha-2 Agonism cause?

A

Inhibits NE release from presynaptic neurons causing decreased BP and HR.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the MOA of TCAs?

A

Na+ channel blockers
Inhibit NE re-uptake
Inhibit serotonin (5-HT) re-uptake
Alpha-1 Antagonist
Anticholinergic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are some examples of TCAs?

A

Amitriptyline, Nortriptyline, and Imipramine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the MOAs of Selective NE Re-Uptake Inhibitors (SNRIs)?

A

Inhibit the re-uptake of NE
Inhibit the re-uptake of 5-HT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are some examples of SNRIs?

A

Venlafaxine and Duloxetime

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is the MOA of Selective Serotonin Re-Uptake Inhibitors (SSRIs)?

A

Inhibit the re-uptake of 5-HT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are some examples of SSRIs?

A

Paroxetine, Fluoxetine, Citalopram, and Sertraline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How do you treat anticholinergic presentations caused by TCAs?

A

Primarily symptomatic +/- benzodiazepines.

Physostigmine
Pyridostigmine

37
Q

How do you treat Na+ channel blockade caused by TCAs?

A

Sodium bicarbonate.

38
Q

How do you treat Alpha-1 Antagonism caused by TCAs?

A

Fluids +/- vasopressors.

39
Q

How do you treat Serotonin Syndrome caused by TCAs?

A

Primarily symptomatic +/- benzodiazepines

Cyproheptadine (serotonin antagonist)

40
Q

What is the MOA of Sodium Channel Blockers?

A

Inhibits the neuron depolarization and action potential propagation leading to the inhibition of neurotransmitter release.

41
Q

What are some examples of Sodium Channel Blockers?

A

Lidocaine and Carbamazepine

42
Q

What is lidocaine used for?

A

Local anesthetic and opioid sparing.

43
Q

What is an adverse effect of lidocaine?

A

Bradycardia

44
Q

What is carbamazepine used for?

A

Trigeminal neuralgia

45
Q

What are some adverse effects of carbamazepine?

A

Toxic epidermal necrolysis (TEN) and Steven Johnson Syndrome (SJS)

Bradycardia
SIADH: hyponatremia
CYP inducer

46
Q

What is the MOA of GABA-B agonists?

A

Decrease presynaptic Ca2+ influx and increase postsynaptic K+ efflux

47
Q

What is an example of a GABA-B agonist?

48
Q

What is the role in therapy of GABA-B agonists?

A

Spasticity

49
Q

What are some adverse effects of GABA-B agonists?

A

CNS depression
Abrupt withdrawal is associated with profound spasticity, hallucinations, fever, seizures, and hypertension.

50
Q

What is the MOA of Calcium Channel Blockers?

A

Block presynaptic Ca2+ channels leading to a decrease in Ca2+ mediated neurotransmitter release from presynaptic neurons.

51
Q

What are some examples Calcium Channel Blockers?

A

Gabapentin and Pregabalin

52
Q

What are the roles in therapy of Calcium Channel Blockers?

A

Neuropathic pain from diabetes
Fibromyalgia
Opioid sparing regimens
Seizures

53
Q

What are some adverse effects of Calcium Chanel Blockers?

A

Dizziness, somnolence, confusion, and ataxia.
Pedel edema.

54
Q

What is the MOA of NMDA Antagonists?

A

Decreases postsynaptic depolarization

55
Q

What is an example of a NMDA antagonist?

56
Q

What role in therapy does ketamine have?

A

Acute pain opioid sparing regimens
Chronic pain
Mood disorders

57
Q

What are some adverse effects of ketamine?

A

Confusion, delirium, dreamlike state, excitement, hallucinations, irrational behavior, and vivid imagery.

58
Q

What adverse effect of NSAIDs is significant for COX-2 selective agents?

A

CV disease (myocardial infarction and stroke)

59
Q

What major endogenous ligands to the mu receptors bind to?

60
Q

What major endogenous ligands to kappa receptors bind to?

61
Q

What major endogenous ligands to delta receptors bind to?

A

Enkephalins

62
Q

What are some examples of full mu agonists?

A

Codeine and morphine
Oxycodone, oxymorphone, hydrodocone, and hydromorphone
Methadone, fentanyl, meperidine

63
Q

What are some examples of partial mu agonists?

A

Buprenorphine and Tramadol

64
Q

What are some examples of mixed agonist/antagonists?

A

Buprenorphine and Nalbuphine

65
Q

What are some full mu antagonists?

A

Naloxone, Methylnaltrexone, and Naltrexone

66
Q

What are some additional properties of morphine?

A

Histamine release (itching/rash)

67
Q

What are some additional properties of methadone?

A

NMDA receptor antagonism

68
Q

What are some notable adverse effects of methadone?

A

QTc prolongation and drug interactions

69
Q

What is methadone used for?

A

Chronic pain and opioid use disorder

70
Q

What are some additional properties of fentanyl?

A

Serotonergic

71
Q

What are some additional properties of meperidine?

A

Serotonergic and anticholinergic

72
Q

What are some adverse effects of meperidine?

A

Serotonergic, anticholinergic, and neurotoxicity

73
Q

What are some additional properties of tramadol?

A

Inhibits the re-uptake of serotonin and NE

74
Q

What are some adverse effects of tramadol?

A

Serotonin syndrome and lowers seizure threshold.

75
Q

What does the mnemonic “With seizures, I BITE my tongue” stand for?

A

Isoniazid, bupropion, imipenem/cilastatin, tramadol, enfluane.

76
Q

What is the MOA of Naloxone?

A

Full mu competitive antagonist that acts centrally and peripherally.

77
Q

What timeline is the duration of action of naloxone?

78
Q

What is the role in therapy for naloxone?

A

Acute opioid overdoses and toxicity.

79
Q

What timeline is the duration of action of naltrexone?

A

Full mu competitive antagonist that acts centrally and peripherally.

80
Q

What timeline is the duration of action of naltrexone?

81
Q

What is the role in therapy for naltrexone?

A

Opioid use disorder (OUD) and alcohol use disorder.

82
Q

What is the MOA of methylnaltrexone?

A

Full mu competitive antagonist that acts peripherally.

83
Q

What is the role in therapy of methylnaltraxone?

A

Opioid use constipation.

84
Q

What is the MOA of Buprenorphine?

A

Partial/mixed mu-agonist that demonstrates a ceiling effect.

85
Q

What is the role in therapy for buprenorphine?

A

Chronic pain and opioid use disorder.

86
Q

What is the MOA of Nalbuphine?

A

Partial/mixed mu-antagonist.

87
Q

What is the role in therapy of Nalbuphine?

A

Opioid-induced pruritis

88
Q

What is Clonidine used for?

A

Treatment of opioid withdrawal

MOD II (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions